Greetings and welcome to the Immunocore Conference Call and Webcast. At this time, all participants are in a listen-only mode. The question-and-answer session will follow the formal presentation. If anyone should require operator assistance, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. It is now my pleasure to introduce Clayton Robertson, Head of Investor Relations. Thank you. You may begin. Thank you. Good morning and good afternoon. Thank you for joining us on our Q4 and full-year 2024 earnings call. During today's call, we will make some forward-looking statements which are qualified by our safe harbor provision under the Private Securities Litigation Reform Act of 1995. Please note that actual results can vary materially from those indicated by these forward-looking statements, including those discussed in our filings with the SEC. On today's call, I'm joined by Bahija Jallal, CEO of Immunocore, who will share a strategy update. Then, Ralph Torbay, Head of Commercial, will review our full-year '24 KIMMTRAK sales and KIMMTRAK lifecycle management plans. David Berman, our Head of R&D, will provide some pipeline updates highlighting near-term readouts in infectious diseases. Travis Coy, our CFO and Head of Corporate Development, will also provide highlights on our financial results reported this morning. Bahija. Thank you, Clay, and good morning, good afternoon, everyone. Our first order of business today is to welcome Travis Coy, our new CFO. This is Travis's first earnings call for Immunocore, and we are delighted to have him join us. He was on our board previously. Welcome, Travis. Today, the team will share the details of our fourth quarter and full-year 2024 performance and the progress of our clinical portfolio. As always, we have been laser-focused on advancing our mission of bringing transformative medicine to patients. I am very proud that 2024 was another year of strong execution thanks to the fantastic work delivered by our teams. We delivered KIMMTRAK to more patients around the world and achieved 5% growth in Q4 versus Q3 and 30% year-on-year revenue growth, culminating in a total of $310 million in revenue for the year. This continues our great track record of commercial execution. In 2024, we also progressed our deep and diverse clinical pipeline with exciting and promising molecules at all stages of development and across three therapeutic areas which could bring new treatment options to patients. We have advanced our three ongoing phase III trials, including the two phase III melanoma trials, TEBE-AM, and ATOM, as we execute on our KIMMTRAK lifecycle management. We also randomized the first patient in our third phase III trial, PRISM-MEL. We remain encouraged by the preliminary data in other tumors and will continue to expand to have the data we need to determine next steps. Our portfolio growth is fueled by an R&D engine that delivers a robust early pipeline. In 2024, we initiated two phase I trials with two novel molecules that David will talk to you about in a few minutes. Expanding beyond oncology, in infectious diseases, we completed the HBV single ascending dose trial, and we will be presenting initial data from the multiple ascending dose portion of our HIV trial later this quarter. Our modular technology allowed us to expand into new therapeutic areas tackling autoimmune diseases. We advanced two autoimmune candidates, one targeting type 1 diabetes and the other atopic dermatitis. These efforts have been delivered by all our employees, guided by an excellent leadership team and supported by a strong balance sheet and disciplined spending. I now ask the team to share additional details. First, Ralph will discuss KIMMTRAK's commercial performance. Ralph, please. Thank you, Bahija, and hello, everyone. KIMMTRAK has had another year of exceptional growth, and I continue to be very proud of our team's dedication to reach more patients globally. KIMMTRAK truly embodies our mission of bringing transformative immunotherapies to patients. We have raised the bar for survival in first-line HLA-A*02:01 metastatic uveal melanoma with unprecedented three-year overall survival of around 27%. Patients who before KIMMTRAK were given 12 months to live are now alive two years, even three years later, with KIMMTRAK. With three Prix Galien Awards and two New England Journal of Medicine publications, among other recognitions, this is what transformational innovation looks like. We take the responsibility of commercializing this transformational medicine very seriously, and last year alone, we launched KIMMTRAK in 14 countries for a total of 24 countries launched. We have also established KIMMTRAK as a center of care across most major markets with over an 80% share of HLA-A*02:01 positive patients. We're continuing our global expansion with KIMMTRAK, which has now been approved in 39 countries, including most recently in Brazil. We have delivered nearly three years of continuous net revenue growth with KIMMTRAK. For the full year 2024, KIMMTRAK generated $310 million in net revenues, which represents a 30% year-on-year growth. In the fourth quarter, we reported $84.1 million in net revenues, representing a 5% increase from the prior quarter. The United States accounted for $226 million, growing at an impressive 34% year-on-year. In 2024, we successfully treated two out of three patients in the community, with nearly half of all new KIMMTRAK patients starting there. We estimate a market penetration of around 65% in the U.S., with a duration of therapy of approximately 12 months. These numbers speak to our efforts and, as importantly, to KIMMTRAK's safety and exceptional efficacy. Looking ahead at 2025, we continue to expect KIMMTRAK's incremental growth driven by three main factors. First, U.S. community expansion focused on less dense areas, leveraging the AI tools we launched last year. Second, duration of therapy, which continues to increase beyond clinical trial experience, highlighting KIMMTRAK's benefit beyond typical resistance progression. And third, new launches ex-U.S., including the recent launch in the U.K. and Poland. We're also excited to potentially expand the benefit of KIMMTRAK to additional indications with our lifecycle management program, which I will take you through in the next slide. No therapy has been proven to extend survival in second-line metastatic cutaneous melanoma post-checkpoint inhibitors. Patient survival in this setting is poor and hovers at around 55% at one year. TEBE-AM is the first phase III trial aiming to show improved overall survival in this setting. There are strong reasons to believe in the potential of KIMMTRAK in this patient population based on phase I trial data that showed a 75% survival rate at one year, as well as an acceptable safety profile. The TEBE-AM trial has three arms: KIMMTRAK monotherapy, KIMMTRAK in combination with pembrolizumab, and a control arm which includes options such as investigator choice of chemotherapy, retreatment with anti-PD-1 or BRAF therapy, or clinical trials. We have line-of-sight data within the next 18 months. Enrollment is on track to finish in the first half of 2026 and data in the second half of 2026. The ATOM trial is the only registrational phase III trial in the adjuvant uveal melanoma setting, with the potential to prolong time to progression and survival. There remains a huge unmet need for patients at high risk of recurrence after definitive treatment, which is often radiation or removal of the eye. Patients currently have no other option but to watch and worry. Yet we know for half of these patients, metastasis will occur within three years. The ATOM trial in collaboration with the EORTC aims to treat patients during this period with the goal of delaying or eliminating metastases. EORTC enrolled the first patient in the fourth quarter of 2024, and the trial is currently recruiting patients globally. As we look to the future for KIMMTRAK, we strongly believe in its potential to help up to 6,000 patients with melanoma live longer. This vision is built upon robust clinical data, groundbreaking phase III trials, and a proven track record in the clinic. We're steadfast on our commitment to transforming patient outcomes and solidifying KIMMTRAK's position as a leading therapy in the melanoma landscape. Now I'd like to pass the baton to David to discuss our promising pipeline. David. Thank you, Ralph. I am pleased to share an update on our clinical portfolio. 2024 was an execution-rich year for our R&D team. We started two phase III trials, PRISM-MEL and ATOM, two phase I trials, PIWIL1 and PRAME HLE, the MAD phase of HIV, and we completed the SAD of our HBV trial. Over the next 12-18 months, we hope to have data readouts, including potentially for TEBE-AM, that will guide next steps for these programs. Ralph has just presented the KIMMTRAK clinical trial updates, and so I will provide brief updates on PRAME, PIWIL1, HIV, and our autoimmune programs. Let's talk about PRAME. We are actively randomizing patients into the phase III study in newly diagnosed metastatic cutaneous melanoma, studying brenetafusp plus nivolumab versus a nivolumab regimen. The goal for this year is for the Independent Data Monitoring Committee to review data on the first 90 randomized patients in order to select between the 40 microgram and the 160 microgram as the go-forward dose. Beyond cutaneous melanoma, we are focused on three goals this year. First, building on the initial signals of activity in ovarian carcinoma, we will study brenetafusp in chemo combinations in platinum-resistant ovarian and in earlier lines in combinations in platinum-sensitive ovarian carcinoma. Second, we will continue signal detection in lung cancer with osimertinib and docetaxel. Third, we will continue dose escalation of our PRAME half-life extended IMC. All three will be reviewed together over the next 12 - 18 months to determine next steps. PRAME and GP100 are both well-known targets for TCR therapies. In contrast, PIWIL1 is a novel first-in-class target, and our ongoing phase I program here demonstrates the power of our discovery engine. Colorectal carcinoma has an increasing incidence and a high unmet need. IMC-R117 is the first immunotherapy to target PIWIL1, a protein expressed in colorectal carcinoma, which we know has historically been insensitive to checkpoints. PIWIL1 is an attractive target since it's not expressed in normal vital tissues, is a negative prognostic marker, and has broad expression in about a quarter of colorectal cancer patients. We designed the phase I dose escalation, which started last year, based on all the insights from our earlier ImmTAC programs. We have learned which signals are markers of activity for our platform, and we hope to see these mature in the next 12-18 months. We know that our ImmTAC platform is validated in cancer, and therefore we have been excited to test whether the same approach of redirecting T cells can be used for chronic viral diseases such as HIV and HBV. While antiretroviral therapy, or ART, has turned HIV into a chronic disease, there remains a large unmet need for functional cure. We estimate over 500,000 people living with HIV across G7 could be eligible for an ImmTAC that could deliver a functional cure for HIV. The challenge for people living with HIV is that while ART does control the virus, when ART is stopped or interrupted, the virus rapidly rebounds and is detectable in the blood at 50 copies per ml, the threshold for detection, on average within two weeks. Furthermore, eight weeks after interruption, the vast majority of people will have over 200 copies per ml. This is the level of virus associated with risk of transmission or infection. However, the fact that some people can control the virus is reason to believe that the immune system may be able to recognize and target HIV-infected cells and supports the hypothesis of our ImmTAC immune therapy approach. In the most recent meta-analysis, which was just published last month, one of the best predictors of HIV control was whether the person started ART early versus late in their infection. The population in our phase I trial generally started ART later after initial HIV infection. Here, the historical rate of HIV control at week 12 is very rare. Our phase I trial is called STRIVE, and we are treating people living with HIV with M113 on the background of ART for 12 weeks and then stopping both therapies. The objectives are to determine whether we can reduce the viral RNA reservoir during the treatment phase and then whether we can alter the kinetics or delay viral rebound after treatment interruption. We will present the initial MAD data from 16 people living with HIV at a conference next month. Over the next 12 months, we will continue dose escalation to be followed by expansion. We know that our tissue targeting platform works based on the KIMMTRAK survival benefit. We came up with the idea of using our tissue targeting platform to turn down the immune system for the treatment of autoimmune disease. Over the next 12 - 18 months, we will bring our two lead autoimmune candidates, one for type 1 diabetes, the second for atopic dermatitis, into the clinic. Our vision for treating autoimmunity is unique, and that is tissue-specific down modulation of the immune system, which would avoid systemic immune suppression. We accomplish this with our ImmTAAI molecule, which has three features. First, the targeting arm, which binds strongly or tethers the ImmTAAI to the target tissue. This provides tissue specificity. Second is a PD-1 agonist that turns off T cells by checkpoint agonism, which is the opposite of checkpoint blockade. And third is an Fc fusion to enable longer half-life for infrequent dosing. These three features are designed to realize our vision of tissue-specific immune suppression. The hallmark of our approach is that the ImmTAAI will only inhibit T cell activity when tethered or bound to the target cell or target tissue. For example, when the ImmTAAI is not tethered, that is, free-floating in blood or other tissues, it is not brought into the T cell synapse and so does not inhibit T cell activation. This avoids systemic immune suppression. However, when the ImmTAAI binds to the target cell, it is brought into the T cell synapse where the PD-1 agonist effector potently inhibits T cell activity. This will result in tissue-specific immune suppression. Type 1 diabetes is a terrible autoimmune disease that requires lifelong insulin replacement and carries risks and morbidities. There remains a high unmet need for well-tolerated medicines to delay or prevent progression of T1D. This is the goal of our first program, IMC-S118. T1D is caused when autoreactive T cells kill the beta cell in the pancreas. These are the cells that normally secrete insulin. IMC-S118 protects against autoreactive T cell killing only when tethered to the beta cell. When not tethered, the ImmTAAI is unable to prevent the killing of the beta cell. We have recently generated exciting ex vivo proof of concept for IMC-S118 in pancreatic slices from a deceased donor who had recent onset of T1D prior to their death. We demonstrated that IMC-S118 binds specifically to beta cells and that it can have an inhibitory effect on the T cells within the pancreatic slice. IMC-S118 is on track for CTA later this year. I will now turn to our second autoimmune program that uses the same PD-1 agonist but employs a different targeting domain and is intended for atopic dermatitis. Langerhans cells and an HLA-like molecule called CD1a that is expressed on Langerhans cells both play key roles in triggering allergic inflammation in the skin. Langerhans cells are sentinels in the skin. They monitor and are the initial triggers to alert the immune system. Two important ways they alert the immune system are by presenting lipids via CD1a and by presenting peptides via class I and class II. Preventing Langerhans cells from initiating pathogenic inflammation via blocking both lipid and peptide presentation may have therapeutic benefit in several important inflammatory diseases, including atopic dermatitis. Our candidate U120 is designed to achieve this goal of dual blockade. The targeting domain recognizes and binds CD1a and thus tethers the ImmTAAI to Langerhans cells. When it does bind CD1a, it sterically blocks lipid presentation, and this prevents lipid-sensing T cells from being activated. By now coating the Langerhans cell in thousands of PD-1 agonist spikes, which is the effector arm, U120 will turn off any T cell that approaches the Langerhans cells to be activated by peptides. In fact, in vitro, U120 is more efficacious than peresolimab, a PD-1 agonist that is not tethered and has lower potency for PD-1 agonism. The next 12-18 months is an exciting time for our R&D teams as we look forward to the conclusion of the phase III TEBE-AM trial, decisions on the next steps for PRAME, PIWIL1, HIV, and HBV, and beginning our journey into developing our platform for autoimmune disease. I would like to welcome and now hand over to Travis. Thank you, David. Good morning, good afternoon, everyone. Earlier today, we released our financial results for the fourth quarter and year ended 2024. Please refer to the press release and our latest SEC filing on Form 10-K for our full financial results. Let me share some of our key financial highlights for 2024 and then touch upon our expectations for 2025. As Ralph mentioned, 2024 was a strong year for KIMMTRAK sales, with net sales growing to $84 million in Q4, a 5% increase versus Q3, primarily driven by volume growth in the U.S. and continued launches outside of the U.S. For the first time, we exceeded full year sales of $300 million, with total sales for the year of $310 million, which represents growth of 30% over 2023. It is worth noting that the reimbursement environment in Europe remains challenging, and we continue to make our best estimates for revenue recognition as we finalize price negotiations. As we continue to invest in our portfolio, SG&A and R&D expenses have increased versus 2023. R&D expenses increased primarily due to investments in our three phase III trials. The phase I/II cohort expansions in ovarian and lung for brenetafusp also contributed to the increase. Our SG&A expenses increased slightly, primarily due to an increase in general business functions needed to support our operations. Moving to 2025, let me provide some comments on how to think about KIMMTRAK sales growth expectations and our SG&A and R&D expenses for this year. For KIMMTRAK, we expect revenue to grow incrementally in 2025, led primarily by growth in the US by further penetration into the community setting and by growth, to a lesser extent, from launches in the EU and international markets. We anticipate that R&D expenses will increase relative to 2024 as we further advance our clinical and preclinical pipeline candidates, and shifting to SG&A expenses, we expect those investments to be mostly consistent with Q4 2024 levels over the course of 2025, while anticipating typical quarterly variability. Turning briefly to our cash position, I am pleased to report that we had $820 million in cash and marketable securities at the end of the year. As a reminder, we repaid our $50 million loan with Pharmakon in November. We believe our robust financial position, coupled with prudent expense discipline and data-driven investments, enables us to advance our portfolio to deliver transformative medicines to patients across all three of our therapeutic areas. I'll now pass the call back to Bahija. Thank you, Travis. Thank you, David and Ralph. We enter 2025 with an eye toward delivering significant results in the next 12-18 months, starting with the HIV MAD data this quarter. This year, we expect incremental growth of KIMMTRAK, will continue enrolling patients in our three phase III melanoma trials, pursue additional opportunities in our PRAME franchise, and continue to develop the next generation of transformative immunomodulating therapies. With our strong financial position, a deeply differentiated portfolio, our dedicated teams, and a clear line of sight for the future, we are confident in our ability to continue delivering significant value to both patients and shareholders. Thank you, and we'll now open the floor for questions. Thank you. We will now be conducting a question-and-answer session. If you would like to ask a question, please press Star 1 on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press Star 2 to remove yourself from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the Star keys. As a reminder, we ask that you please limit yourself to one question. One moment, please, while we poll for your questions. Our first question comes from the line of Michael Yee with Jefferies. Please proceed with your question. Hey, good morning. Thanks for the question. We had a question on the upcoming HIV results, which David made a bunch of comments on coming up, and we wanted to understand in the 16 patients, would they all have 12 weeks or so off therapy, off all the therapy? And so you would have a clear picture of whether there would be viral rebound over an extended period of time and what you would deem to be a good rate of patients not rebounding. And then a follow-up question is a quick housekeeping question. Maybe the company could comment on the European sales, which appeared to be down sequentially Q4 to Q1. Was there some one-time adjustment on price or lumpy ordering patterns? What was going on there? Thank you. Great. Thank you. David, do you want to take the first one? Michael, thank you very much. Yes, all patients will have been off of therapy and entered the ATI, and all will have been available to see whether there is antiviral activity and, of course, whether there is a viral reservoir reduction during the treatment phase. In terms of your question of what rate is good, I would just remind you that this is a phase I dose escalation with five to six people per cohort. So I wouldn't focus necessarily on rates at this point. I think we need to get to a top dose and then expand. But in terms of a TPP, Michael, I would point you to a recent publication a few years ago in terms of what they would like to see in terms of rates and in terms of what good looks like. And essentially, it is copies. They would like to see suppression of viral copies to less than 200 copies per mL for two years in about 20%-30% of people. That's the minimum commercially successful TPP. Ralph, do you want to address the Europe? Happy to. So as Travis mentioned, Michael, Europe is having a challenging reimbursement environment. And as you know, we are negotiating prices with Germany and France. We actually have slight insight on those negotiations. We had 14 successes worldwide, which speaks to sort of how well we're doing. And we have some incremental growth as we've been guiding, basically, in Europe, which is what is reflected in our numbers. Thank you. Our next question comes from the line of Jessica Fye with J.P. Morgan. Please proceed with your question. Hey, guys. Good morning. Thanks for taking my question. So maybe following up on Mike's question for HIV, can you elaborate on what factors are going to help you determine a go-forward dose and how you would think about next steps once dose escalation is complete? Would you move directly to a registrational trial? What could something like that look like? Thank you. Yeah. Jess, thank you for the question. So in terms of the factors we would use to select a go-forward dose, of course, safety. This is a relatively healthy population, so it needs to be a well-tolerated regimen, and then we need to see that we have evidence of antiviral activity that gives us reason to believe that we can achieve a functional cure. Right now, we selected 12 weeks of dosing. We're focused on the dose. There might need to be to optimize frequency. There might need to be duration. We'll also look, of course, at biological activity. So we'll use all of those. And there might, by the way, be two doses that we take forward into an expansion. In terms of the next steps after an expansion, once we've confirmed a signal, typically, there's a randomized phase II with a placebo. And that would then lead to a phase III trial. Now, interestingly, the meta-analysis that was just published, and I refer everyone to that last month, they're trying to argue that you don't need to do a placebo-controlled randomized phase II anymore because the historical rate of control is actually quite low. So that meta-analysis argued for doing single-arm trials, but that's something we'll consider as we approach them. Yeah. And we definitely will talk to the regulatory authorities before we do anything. Thank you. Our next question comes from the line of Tyler Van Buren with TD Cowen. Please proceed with your question. Hey, guys. Good morning. Thanks very much. I'll ask another one on HIV just for additional clarity. It's been very helpful what you've said already. But just the 12-week time point of patients being controlled following ART interruption, is that enough to have confidence that they would maintain control over the longer term, or do you need to follow them longer? And at which point would you have confidence based upon KOL feedback? And I guess related to that, have strategics told you what profile they would like to see demonstrated in the clinic or what level of follow-up is required as well? Tyler, the 12 weeks of interruption is historically being used in these initial phase I trials to get a sense of whether you have any activity because based on the meta-analysis that I mentioned, the percentage of people who will have viral control at 12 weeks is about 1%. It's extremely low. When you're conducting these trials, you don't want to keep the people off of therapy for too long, especially in the initial phases. You first want to look for 12 weeks to see if you have evidence of antiviral control. You then move to expand those 12 weeks. In terms of what is commercially acceptable or target product profile, and I would add that no therapy or company or anyone has been able to demonstrate viral control reliably. This is a new area that there is no precedent to base it on. I would really refer you to that white paper that published what a commercially successful TPP, what the minimum case is, and what the base case is. Thank you. Our next question comes from the line of Eric Schmidt with Cantor Fitzgerald. Please proceed with your question. Thanks for taking my question. Maybe I'll mix it up a little bit and ask a question on brenetafusp and the PRISM-MEL study, the dose selection that's going to happen, I guess, later this year. On those first 90 patients, what kind of follow-up will you have in terms of duration? And I assume you're going to make a decision on early disease control. Is that feasible given the follow-up? I'm also kind of curious as to whether we'll see updated phase I data on brenetafusp and second-line melanoma this year. Thank you. Yeah. I'm happy to take that. So the way the 90-patient dose selection analysis is set up is that those patients will be followed up for between eight and 12 weeks. So really, it's looking at a high level for both safety as well as initial response rate. And it's really set up to look for big differences because we know that both doses are active. Thank you. Our next question comes from the line of Justin Zelin with BTIG. Please proceed with your question. Good morning, and thanks for taking our question and congrats on all the progress. It's great to see the progress in the pipeline outside of oncology. I want to ask how you expect the safety and tolerability profile of ImmTACs outside of the oncology settings, such as in the infectious disease or autoimmune disease settings, to shake out. And what would be the minimum commercially successful TPP that would be in these settings in regards to adverse events, such as CRS? Thank you. Yeah, Justin, happy to take it. It's a very good question. In terms of infectious disease, what we would expect to see, of course, is cytokine release syndrome because that's the mechanism T-cell activation leads to cytokines. But in contrast to oncology, we can't really have moderate or severe CRS. So we really need to only have mild CRS. And we think that's really achievable. We don't expect to have any on-target off-viral activity because these are viral peptides that aren't in the body. So in contrast to GP100, we see rash. We don't expect to see any other toxicity aside from mild cytokine release syndrome. And I think that's what would be needed in HIV and HPV where the people are generally healthy. In terms of autoimmune, actually, we don't expect to have any right now. We don't expect to have cytokine release syndrome because we're turning off the immune system. We're not turning it on, and the other nice feature of our platform is it's intended to be tissue-specific. So any immune suppression we see will be localized in the target tissue. We shouldn't expect to see broad systemic immune suppression. In fact, that's one of the differentiating features. So in the autoimmune, we're looking in autoimmune and in HIV, we're looking for very infrequent dosing that is very well tolerated. Yeah. I just want to add to this. I think you see in HIV, we did actually share that we are escalating beyond 300 micrograms, just to give you an idea. So I think the safety profile is very good. Thank you. Our next question comes from the line of Craig Suvannavejh with Mizuho Securities. Please proceed with your question. Hi, this is Sam on for Craig. Thank you for taking our questions. Maybe going back to brenetafusp, can you provide an update on the current efforts to generate data in ovarian and lung cancers? What were the changes that have been made in patient recruitment in those indications? And when might you be able to share next data? Thank you. I'm happy to take that, Sam. So with ovarian, we're building up the initial signals. It was clear that brenetafusp had monotherapy activity and late-line platinum resistance, but we needed to see a path forward. And that path forward is in earlier lines and in combinations. We saw an interesting signal for chemo combinations in the platinum resistance. So we need to expand platinum-resistant chemo combo. And then we need to study platinum-sensitive bevacizumab. And those are ongoing now. In the lung setting, we're more in the signal detection phase here. And so here, we're looking at combinations with osimertinib and docetaxel, which are generally earlier lines than the late-line PROC. And so we hope to see signals there. In terms of when we're going to share the data, we're going to share the data when there's a complete understanding of what's going on and we have a story that we can put together. So I don't want to nail it down, presumably in the next 12-18 months. Thank you. Our next question comes from the line of Jonathan Chang with Leerink Partners. Please proceed with your question. Hi, guys. Thanks for taking the question. How are you guys thinking about business development opportunities for 2025? Thank you. Great. Thank you. Travis? Yeah. No, thanks for the question. So first of all, we're obviously very excited about the opportunities we have in the pipeline currently. At the same time, we do continuously look for opportunities to enhance the value of the portfolio. Those opportunities need to be a good strategic fit that leverage our expertise and our capabilities. But we're in a strong position with what we have today. And having that optionality to pursue partnerships at the same time is a great benefit. Thank you. Our next question comes from the line of Michael Schmidt with Guggenheim Partners. Please proceed with your question. Hi. Thanks for taking our question. This is Paul on for Michael. For KIMMTRAK, just on the commercial performance, I believe you've been at or around 65% U.S. penetration for the past couple of quarters. How much additional headroom do you see there in terms of share of that market with your push into the community setting? Where do you see that share in the U.S. market plateauing? And then on treatment duration, you mentioned trending over 12 months. What's your best estimate of where that could land longer term? Thank you. Great Ralph, I think it's 65%, but go ahead. Thank you for the question. As you said, we are at 65% penetrated, which is good news because we've been growing significantly, 34% growth last year in the U.S. Look, we're continuing our work into the community where the good news is that half of our new start prescriptions are coming from the community. In fact, two-thirds of our prescriptions are coming from the community. We just have to continue that work. There is still a lot of patients out there with an unmet need. We're going to continue that work. In terms of the duration of therapy, the duration of therapy is performing better than we've seen in clinical trials. It's difficult for me to predict where this is going to land. We'll see it hopefully grow together. Yeah, which is really unusual, actually. It speaks highly of the treatment, the impact of KIMMTRAK. Thank you. Our next question comes from the line of Jack Allen with Baird. Please proceed with your question. Hey, this is Nigel for Jack. Thanks for taking my question. Surrounding the pivotal first-line PRISM-MEL study of cutaneous melanoma, Piers, you're now specifying timeline for dose selection decision, second half of 2025. It seems like 8- 10 weeks minimum follow-up is expected to be reviewed by the IDMC. What metrics do you expect the IDMC will use to make a dose selection decision, whether that's ORR, ctDNA, or PFS? And to what extent will the interim data be communicated to the company? And finally, can you comment as to whether there was a futility analysis included as part of the dose selection decision? And thanks. So I can start. So we are not intending to release the data just for the integrity of the trial. That's going to be the IDMC looking at it. They're the only ones looking at the trial. But David, do you want to comment? Thank you. There will not be a futility analysis. The analysis is strictly to choose a dose. And that will be done by the IDMC in terms of what will be used. The IDMC will use both efficacy and safety. I would just remind you that in the phase I trial, both doses were active and well tolerated, 40 and 160. And we didn't really see a dose response. So they're going to be looking for large differences. And if they don't see large differences, then they'll be using modeling. We'll be providing support by modeling to help select the dose. Thank you. Our next question comes from the line of Gil Blum with Needham & Company. Please proceed with your question. Yeah, hi. Thanks for taking our question. This is Ethan on for Gil. So you mentioned some reimbursement challenges in Europe for KIMMTRAK, which isn't very surprising. But I know it's early on, but do you anticipate similar challenges for brenetafusp in Europe? Or are these challenges more product indications specific to KIMMTRAK? Thank you. Yeah, I think I'll start. And then Ralph, please comment. I think we are actually. I'll look at the cup half full. We had so far good negotiations and 14 approvals for the drug. But as you know, Europe in general is country by country. And that's what you have to do. And it's more challenging right now. But I want to point out to the fact that we actually overturned the NICE decision. And we got now we're launching in the U.K. That's one of the toughest markets. But Ralph, you want to comment? So as Bahija said, yes, we've had a lot of successes with KIMMTRAK. And that speaks to the value proposition of KIMMTRAK. Look, I think the market is challenging or the reimbursement landscape is challenging for all companies. And you've seen this communicated by everybody. So all we can do is expect good data and keep working to create access for patients across Europe. And hopefully, we'll have the same successes of the data with Brenetafusp businesses like the KIMMTRAK data. Yeah. And for brenetafusp, we expect the same thing. I think if we are lucky and have an OS endpoint that facilitates things in Europe, that's exactly what happened with KIMMTRAK. Thank you. Our next question comes from the line of Peter Lawson with Barclays. Please proceed with your question. Great. Thank you so much. I apologize. I joined the call late. But I'd just love to know around the HIV data that's coming up, how we should be thinking about the bar for success, whether it's around viral reservoir reduction or the delay in viral rebound? And if you can say around that and kind of doses we should expect to see and number of patients in each dose? Thank you. Peter, we expect we will show three doses, five to six people per dose. We are, by the way, continuing to dose escalate now that that data is just not ready for the data cut for the presentation. In terms of what success would look like, this is a setting both viral reservoir reduction during the treatment phase and then demonstrating viral control after interruption. It's never been reliably shown for any therapy. So for us, what we're looking for in a phase I dose escalation is do we have signals of activity? Can we reliably reduce the reservoir? And can we alter the kinetics? To me, that would be a huge success to the field, actually, because no one's been able to show this. Once we complete dose escalation, we then move to expansion. And there we want to get a better sense on percentage of patients who would have antiviral control. And is there enough strength to move forward to randomized phase two trial? So that information will come later this year. Thank you. Our next question comes from the line of Patrick Trucchio with H.C. Wainwright. Please proceed with your question. Thanks. Good morning. My question is also on the HIV program. I was just curious if, based on the data that's generated in this MAD portion of the STRIVE trial, you might see a potential for a combination strategy for M113V, such as pairing it with LRAs. And separately, just based on the outcome of this MAD portion, is there a possibility that M113V could qualify for priority review or other regulatory incentives for a potential accelerated development path? Yeah. Patrick, thank you for that question. And it's a good one because it reminds me that pretty much our entire platform, oncology, HIV, and potentially autoimmune, is combinable. In fact, the phase I trial that we'll share data with in the next few weeks is on the background of ART. And certainly, this could be combined with LRAs. It could be combined with anything, essentially. But the goal for here is not to have chronic long-term treatment. It's for it to have a finite dosing regimen so that we can stop treatment and the patients can be off all therapies for two to three years. I think that would be kind of our eventual. In terms of health authority interactions and priority reviews, I think that is certainly something we would consider once we need to, but we need to generate the data. And so that would come with. It's still too early, I think, to comment on that. Thank you. Our next question comes from the line of Rajan Sharma with Goldman Sachs. Please proceed with your question. Hi. Thanks for taking the question. Just a couple left from my side. Atopic dermatitis, I know that it's a way out until we see the initial data. But just at this point in kind of thinking about your planning for the asset, how are you thinking about potential benchmarks longer term? And then secondly, just on HBV, conscious that we obviously have the HIV update coming relatively imminently. Is there anything from the HIV dataset that you'd be looking to maybe increase confidence in the platform more broadly? And if there's any crossover to HBV there. Thank you. Yeah. Again, in terms of the atopic dermatitis, I think right now we have a lot of excitement about the mechanism in atopic dermatitis because of the role that CD1a and Langerhans cells play in skin inflammation. Our initial entry point will be in patients who are refractory to all therapy because we're going to be looking for a signal. And I think after that, at that point, we'll probably be in a better sense to understand what a commercially acceptable TPP is. In terms of the HIV data, which is next month, and then the HBV, I think you asked about that, SAD data, I actually look at them as a package. And I think they are both important because they are the first time TCR therapy has been used in HIV and first time in off-the-shelf TCR therapy in HBV. And so I think, although the HBV is SAD data, the question there is we're going to be asking, can we see anything after a single dose? I think it's a hard hurdle, but can we see anything? So I think those two data pieces this year will be important to understand whether ImmTAC can work in chronic viral diseases. Yeah. Just to add, I think on CD1, there are multiple indications, and I think that's the attractiveness about the mechanism, and both HIV, HBV gives us higher confidence for the platform to work in infectious disease and a lot of learning there. Thank you. Our next question comes from the line of David Dai with UBS. Please proceed with your question. Great. Hey, thanks for taking my questions. Just one from me. So regarding HIV program, I just want to dig into the mechanism of action. Could you maybe highlight some of the preclinical data that gives you confidence of potential viral control for the phase I trial? Thanks. David, sure. So we've actually published several papers on the preclinical data. It's actually quite fascinating. So we've shown that this molecule can redirect T cells to kill HIV-infected CD4 T cells. So we've shown that in vitro. We've actually shown imaging, microscopy showing that the ImmTACs can bridge a T cell to an infected CD4 T cell, so a CD8 killer cell to an infected CD4 T cell. And we've shown that this can work even when you don't kick with the HDAC inhibitor, you don't have to activate the T cell to induce transcription of the HIV expression. So we do have some interesting preclinical data. We're happy to share those publications. But there is a body of evidence we've already published. Yeah. And I think the one reason for this platform and for the HIV, we know that the reservoir has very low expression, if you will, of the target. And we know that our technology can kill cells down to five to 10 targets or copies per cell. So that's another reason to believe. Thank you. Our next question comes from the line of Jeff Jones with Oppenheimer. Please proceed with your question. Hi, guys. And thanks for taking the question. Just one from us. In terms of the autoimmune program and AD being your first universal program, how are you thinking about applicability of that to the oncology programs? Thanks. Yeah. I would say that what they have in common is the tissue targeting part, that we can show exquisite tissue targeting with our cancer program. And we believe we'll get exquisite tissue targeting with our autoimmune program. Where they differ, of course, is in the effector side. In oncology, we're activating T cells. In the autoimmune, we're turning T cells off. And so they differ in that regard. But they both have in common the TCR targeting. And in fact, our preclinical toxicology de risking program that we're going to use for autoimmune does incorporate many of the aspects we use for oncology. Yeah. The way I think about it is the yin and yang, if you will, of the oncology and autoimmune. And that's another reason why we are in both areas, therapeutic areas. Thank you. There are no further questions at this time. I would now like to turn the floor back over to Bahija Jallal for any closing remarks. Yes. Thank you, operators. I just want to thank you again for dialing in, for excellent questions, and for your support, and have a great day. Thank you. This does conclude today's teleconference. We appreciate your participation. You may disconnect your lines at this time. Enjoy the rest of your day.